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VIRUS
Herpesvirus-1
(HSV-1)
Herpesvirus-2
(HSV-2)
FAMILY
Alpha herpesvirus
(latent in sensory
neurons)
Alpha herpesvirus
(latent in sensory
neurons)
ENVELOPE
STUFF TO KNOW
yes
IE (immediate early) proteins - bind DNA, regulate transcription
E (early) - transcription factors, DNA polymerase, thymidine
gD is main
kinase (TK)
glycoprotein; L (late) - structural proteins, glycoproteins, envelope coat
gp's B, D, H, L -DNA replicates in nucleus, but envelope received in cytosol
for attachment -gp's + tegument = envelope
and infectivity! Pathogenesis: CTL mediated response
-evades endosomes → released in infectious form!
-virus migrates to sensory ganglia during primary infection, lives there
until reactivation: during stress, vesicles appear again, may be due
to a deficiency in IFN-γ
-blisters contain multinucleated giant cells and intranuclear inclusions
Receptors: heparan sulfate, Hve A,B,C,M, Nectin 1,2,
Diseases: virus + immune response (although many are asymptomatic)
1. Gingivostomatitis - swollen vesicles on mucous membranes
2. Whitlow - watery finger pustule spread from primary infection
3. Keratitis - corneal infection, very common cause
4. Encephalitis - fever, personality change, focal seizures
5. Eczema herpeticum - in presence of underlying eczema
Latency = transcription but no translation
yes
gD is main
glycoprotein
pathogenesis same as HSV1, just antigenically distinct (diff. gp's)
genital infection, usually with self-limited meningitis
Diseases:
1. neonatal infection - transplacental viral transfer, attack rate higher
if mother is newly infected near time of birth (otherwise do C-section)
a) skin and mucous membrane infection - skin rash, DIC if untreated
b) CNS infection - fever, lethargy, seizures, CSF abnormal
c) disseminated - hepatosplenomegaly, jaundice, high mortality!
TREATMENT/
VACCINE
immunofluorescence,
culture, PCR
topical acyclovir, or
start IV if suspect
encephalitis, even
before results come
back!
Ribavarin
no vaccine
immunofluorescence,
culture (24-48 hrs),
PCR
acyclovir, oral or IV
(fam or valacyclovir
is oral)
no vaccine yet
VIRUS
Varicella-zoster
virus (VZV)
Cytomegalovirus
Epstein-Barr virus
FAMILY
Alpha herpesvirus
(latent in sensory
neurons)
ENVELOPE
yes
gE is main
glycoprotein
Beta herpesvirus
yes
(latent in lymphoid
and other cell types gB and gH
like salivary glands
and the kidney)
Gamma herpesvirus yes
STUFF TO KNOW
no asymptomatic shedding, only infectious when clinically apparent
can be transmitted during pregnancy and delivery - give newborn IgG
cell-mediated immune response most important
Pathogenesis: inhaled virions infect respiratory mucosa
-cell-cell spread only, unless talking about skin vesicles - enveloped
infectious virions produced in vesicles
-T lymphocytes infected, viremia ensues, get skin vesicles
-virions in vesicles migrate up sensory root and are latent in ganglia
only to reappear in zoster
-lytic infection, regulatory protein expression nuclear; latent infection,
regulatory protein expression is cytoplasmic
-ORF 62 (open reading frame) protein is critical in formation of new viruses
and maintenance of latent infection
Receptors: heparan sulfate, mannose-6-phosphate receptor
Diseases:
1. Varicella (chickenpox) in children - skin vesicles (adults are 25x
more likely to have severe disease)
2. Zoster (shingles) in adults only as reactivation of latent VZV
rash distributed along sensory nerve root one on side of body
3. Post-herpetic neuralgia, a rare development after zoster reactivation
Pathogenesis: infection is through saliva, tears, urine, sexual contact
-not airborne! no skin lesions
-infectious virus can persist on table-tops → day care problem
-latent in bone marrow precursors of monocytes
-down-regulates MHC class I, evades immune system
Diseases:
1. self-limited mono in immunocompetent patients
2. CMV infection in immunocompromised - pneumonia, fever, retinitis,
colitis, lymphadenopathy, rash, encephalitis, neutropenia
-reactivation common in transplant pts, AIDS pts
3. Congenital CMV - transfered during pregnancy, risk highest during
1st trimester. If acquired at birth, disease not as bad.
Pathogenesis: asymptomatic people shed virus in saliva
-lytic infection, tumor virus
gp350 binds to -evades immune system with 1L-10 mimics, ↓ IFN, inhibits apoptosis
CD21 on B
-latent EBV lives in memory B cells
cells
Diseases:
1. Infectious mononucleosis - fever, malaise, pharyngitis, myalgias,
lymphadenopathy, hepatosplenomegaly
2. Nasopharyngeal carcinoma
3. B-cell lymphoma
4. Leiomyosarcoma
5. Oral hairy leukoplakia in AIDS pts
6. X-linked lymphoproliferative disease (in males only)
TREATMENT/
VACCINE
culture (5-7 days)
immunofluorescence
PCR
acyclovir, oral or IV
(famciclovir or
valacyclovir for elderly
with zoster)
vaccine is live
attenuated, 85%
effective - contraindicated
in immunocompromised
tissue culture looks
inclusion bodies,
immunofluorescence
no acyclovir! Use
ganciclovir, foscarnet,
cidofovir
no vaccine
(+) heterophile test
monospot test =
Viral capsid antigen (VCA) early test
EBV nuclear antigen(EBNA) late test
no good treatment
steroids for
complications
no vaccine
VIRUS
FAMILY
ENVELOPE
Kaposi Sarcoma
Gamma herpesvirus yes
herpes virus (HHV8) (latent in lymphoid
cells)
Influenza A
Orthomyxoviridae
yes
STUFF TO KNOW
only appears in immunocompromised patients
strongly linked to male-male sex
Pathogenesis:
-pirated human genes for it's own repertoire, such as IL-6, Bcl-2,
chemokine genes
Disease: oncogenesis is via transformation
1. Kaposi's Sarcoma in AIDS pts
2. primary effusion lymphoma = body cavity B-cell lymphoma
3 Castleman's disease - malignant lymphoproliferative disease
8 segments of RNA, so can shift and drift! Shift causes major epidemics - if one cell
infected with two strains, they can mix - not recognized by any human antibodies
RNA replicates in the nucleus, which allows for easier antigenic shifting / drifting
A has greatest mutation rate
Virulence:
-HA is hemagglutinin glycoprotein, binds sialic acid residues on host cells like RBCs
sticks out of viral outer membrane; anchored by M-proteins
-NA is neuraminidase protein, cleaves mucin neuraminic acid, exposing sialic acid
residues beneath so HA can bind; also anchored by M-proteins
-M1 protein anchors HA and NA, provides stability
-M2 becomes ion channel in endosomes once endosome is acidified - acid activated
-also has viral polymerase, nucleocapsid, and nonstructural proteins
Pathogenesis:
Tryptase Clara (protease) secreted by non-ciliated Clara cells in bronchial epithelia cleaves
HA into 2 subunits, which allows fusion of virion and host cell membrane
viral HA attaches to host cell and is endocytosed
once endosome is acidified (via M2 in influenza A), virus uncoats
viral RNA is released and transported to nucleus, mRNA is transported out of nucleus
and translated; copies of RNA with ribonucleoprotein also transported out of nucleus
HA and NA brought to surface of host cell and stick out, M proteins accumulate,
packaged RNA is incorporated and virion buds off
Disease:
1. Influenza - fever above 101˚F; myalgia, chills or malaise; cough or respiratory discharge
abrupt onset, lasts for 2-4 days but some symptoms can persist for 2 weeks
a) complications: pneumonia, either viral or bacterial
-if viral, can be from actual influenza - lower tract involvement, can be fatal in young adults!
-if bacterial, two most common infections are S. pneumo and Staph aureus - can be fatal,
especially in older adults and pts with chronic medical conditions
-also neurological - post-infectious encephalitis - self-limited
TREATMENT/
VACCINE
treat with chemo or
radiotherapy
no vaccine
clinical symptoms,
nasopharyngeal
swab or rapid antigen
test
Amantadine,
Rimantadine (interfere
with viral uncoating)
only for flu A;
Zanamivir (inhaled-bad for
asthmatics)
and Oseltamivir (oral)
good for A and B, work by
inhibiting NA protein;
Ribavarin interferes with
mRNA, stops RNA
polymerase
2 vaccine:
injected is whole
killed;
inhaled is live
attenuated
VIRUS
Influenza B
FAMILY
Orthomyxoviridae
ENVELOPE
yes
STUFF TO KNOW
segmented RNA , so can shift and drift
no M2 protein!
Pathogenesis basically same as above
Disease same as above
-can have myositis as complication of Influenza B
TREATMENT/
VACCINE
diagnosis same as
above, can also use
DFA
neuraminidase inhibitors
effective for
flu A and B
yes
yes
Influenza C
Orthomyxoviridae
yes
segmented RNA, but not associated with significant morbidity/mortality
no NA protein! No real shift associated with flu C
see above for general info about influenza
Parainfluenza virus
Paramyxoviridae
yes
Disease:
1. respiratory infections that are a little milder than flu - rhinitis, pharyngitis, sinus
congestion, bronchitis and flu-like symptoms
2. Croup - infection of larynx and upper resp. tract, coughs sound like barks
Ribavarin
occurs in winter months
Th2 response - cell-mediated immune response most important
Virulence: glycosylated surface proteins F (fusion), G, and SH mediate attachment & fusion
-proteins N, L, P assc. with nucleocapsid, M (matrix) proteins, NS (nonstructural) proteins
which may play a role in RNA replication
Pathogenesis: inoculation is via eyes or nose, infection limited to respiratory tract
-G and SH mediate attachment to host cell
-F protein helps virion fuse
-replication of RNA and formation of mRNA
-virion assembly and budding
-if lower tract involvement, atalectasis and trapped air, especially in young children
-easily transmissible, reinfection is common b/c immunity is not complete
Disease:
1. Bronchiolitis in infants - nasal congestion, sore throat, fever, increased RR, can see
retraction of intercostal muscles (means lower tract involvement); lungs are hyperinflated
-duration = 7-21 days
2. Pneumonia in adults - nasal congestion, cough - significant mortality! 20% in older pts
characteristic
formation of syncytia
(fusion of multi-nuc
giant cells)
Respiratory
Syncytial virus
Paramyxoviridae
yes
no vaccine
-aerosolized Ribavarin
(interferes with viral
RNA polymerase)
can be given to high
risk pts, but is
teratogenic
-treat high risk infants
with RSV-Ig or
Palivizumab
(monoclonal
RSV antibody)
no vaccine
Adenovirus
Adenovirus
no
transmission by respiratory droplets, fecal-oral route, and direct contact
outbreaks occur in crowded conditions
Pathogenesis: capsid contains a fiber that helps the virus attach to host cells
Diseases:
-pharyngitis, conjunctivitis, cystitis, pnuemonia, gastroenteritis
Ribavarin
only military uses vaccine
VIRUS
Rhinovirus
FAMILY
Picornavirus
ENVELOPE
no
uses ICAM-1
as receptor
Rabies virus
Rhabdovirus
yes
STUFF TO KNOW
occurs in early fall and spring
optimal growth at 33˚C, which is temperature of nose and large airways
can survive on environmental surfaces for hours - efficient transmission
Virulence: noncytolytic - host immune response is responsible for most of symptoms
-many differect serotypes, so vaccine not really possible
Pathogenesis:
-virus enters via nasal or ophthalmic mucosa
-replication occurs in lymphoepithelial cells in nasopharynx - no viremia
-usually upper respiratory infections, but can involve lower tract
-IL-8 released from infected cells causes more rhinorrhea and nasal congestion
Disease:
1. Common cold! sneezing, coughing, rhinorrhea, nasal congestion, pharyngitis - 1 week
-high fevers, myalgias, chills are not commonly seen
-green nasal discharge not indicative of bacterial infection! color is from myeloperoxidase
a) also acute sinusitis, otitis media, exacerbations of chronic bronchitis, asthma attacks
transmission via bite from infected animal
100% fatal if untreated! high neuroinvasiveness, high neurovirulence
Virulence: RNA encodes:
L protein (polymerase) - capping, methylation
P protein - transcriptional activator
M protein - bridges RNA and envelope
N protein - wraps the template
G protein - antigenic glycoprotein spike
Pathogenesis: virus enters through a break in the skin, across a mucosal surface or inhaled
-virus replicates and infects muscle spindle → infects nerve to muscle, travels centrally
-once it reaches the spinal cord, virus spreads to CNS with almost every neuron infected
-after CNS spread, there is peripheral spread to the rest of the body (saliva, stool, etc)
Disease:
1. Rabies - incubation may be 1-week to a year! biphasic
a) febrile prodrome followed by excitation phase
b) paralysis - paresthesias at site of bite, spasm of laryngeal muscles, coma, paralysis
inevitable death
Vaccine does not work if clinical symptoms have already started.
TREATMENT/
VACCINE
clinical symptoms
treatment is
symptomatic - treat
with over-the-counter
cold remedies
not antibiotics!!
no vaccine
diagnosis uses RT-PCR
of brain, Negri bodies
in brain tissue, CSF
culture, urine, saliva
treatment is postexposure prophylaxis
(vaccine + Rabies Ig)
2 vaccines:
whole killed administered
at 0, 3, 7, 14, 28 days;
or passive Ig shot
injected at site
VIRUS
Poliovirus
Coxsackievirus
Echovirus
FAMILY
Picornavirus
(enterovirus)
Picornavirus
(enterovirus)
Picornavirus
(enterovirus)
ENVELOPE
no
no
no
STUFF TO KNOW
Pathogenesis: enteroviruses enter through GI tract from fecally contaminted material
-virus replicates in submucosal lymphatic tissues in gut
-virus penetrates host cells, uncoats, and releases RNA into cytoplasm
-4 viral capsid proteins and 8 non-structural proteins are transcribed
-inhibition of host cell protein synthesis
-release not necessarily cytolytic
-minor viremia in lymphatic tissue, major viremia in bloodstream
-polio specifics: hematogenous spread to CNS motor and autonomic neurons (not sensory)
attacks gray matter of anterior horn and motor nuclei of pons ans medulla
Disease:
1. Asymptomatic - 95%
2. Abortive poliomyelitis - fever, headache, abdominal pain, anorexia - self-limited
3. Nonparalytic poliolyelitis - looks like aseptic meningitis
4. Spinal paralytic poliomyelitis - 0.1% - biphasic illness
a) minor: looks like abortive polio, lasts a few days, then well for 2-5 days
b) major: headache, fever, vomiting, neck stiffness, muscle pain relieved by motion
results in weakness and eventually flaccid paralysis (can be 1 muscle or many)
5. Bulbar paralytic poliomyelitis - paralysis of cranial nerves, usually IX and X
6. Polioencephalitis - rare, can occur in infants; changes in mental status
infections occur in late summer, early fall
replication, pathogenesis and epidemiology same as polioviruses
Disease:
1. Aseptic meningitis - common in children - fever, followed by headache, stiff neck, URI
self-limited, all pts recover
2. Summer cold - rhinorrhea, sore throat, etc.
3. Encephalitis (rare) - lethargy, seizures, but excellent prognosis
4. Hand-Foot-and-Mouth disease - fever and vesicles in mouth, hand, feet; mouth pustules
help differentiate between this and chickenpox; very contagious!
5. Herpangina - vesicular rash in oropharynx; fever, vomiting, sore throat, painful to swallow
6. Transient paralysis - flaccid paralysis
7. Epidemic pleurodynia - sharp muscular pain with spiking fevers after each paroxysm
8. Myopericarditis - inflammation of heart muscle; virus replication in myofibers → necrosis
seems to attack young adults, esp. males; can lead to dilated chronic CHF
9. Neonatal myocarditis or hepatitis
infections occur in late summer, early fall
replication, pathogenesis and epidemiology same as polioviruses
Disease:
1. Aseptic meningitis - fever, followed by headache, stiff neck, URI
2. Summer cold - rhinorrhea, sore throat, etc.
3. Chronic meningoencephalitis only in patients with defects in B-cell function - can be fatal
4. Transient paralysis
5. Acute hemorrhagic conjunctivitis - pain, swelling of eyelids - contagious, bilateral!
6. Myopericarditis - inflammation of heart muscle; virus replication in myofibers → necrosis
seems to attack young adults, esp. males; can lead to dilated chronic CHF
7. Neonatal myocarditis or hepatitis
TREATMENT/
VACCINE
diagnosis from throat
secretions in 1st week
of illness;
can't use CSF;
serology
no treatment
2 vaccines:
OPV (oral) can revert to
wild-type, also assc. w/
paralytic dz;
IPV (inactivated) given
IM as series of 4 shots
CSF is clear with PMNs
at first, then lymphos
(glucose + protein nl) culture or PCR
treat symptomatically
no vaccine
PCR, viral culture
symptomatic treatment
no vaccine
VIRUS
Rotavirus
Rubella virus
Calicivirus
FAMILY
Reovirus
Togavirus
Calicivirus
Coronavirus (SARS) Coronavirus
ENVELOPE
no
yes
no
yes
STUFF TO KNOW
segmented RNA, but major antigenic shifts don't occur
infections occur during 3-4 months in winter
responsible for 10-20% of all diarrheal-related deaths in children
spread by fecal-oral route, resistant to stomach acid since no envelope
Pathogenesis:
-since ds RNA, must package own RNA polymerase to make mRNA
-binds to sialic acid residues
-once swallowed, infects mature villus epithelial cells of small intestine → death of cells
leading to decrease in absorptive area, may result in lactase deficiency
Disease:
1. Gastroenteritis - vomiting and watery diarrhea, nausea, high fever
TREATMENT/
VACCINE
clinical diagnosis
ELISA or PCR to
detect rotavirus in
stool
supportive treatment
with fluids, don't use
anti-diarrheals
Rotashield vaccine
pulled from US market
transmission via respiratory droplets
envelope contains HA (hemagglutinin) protein and F (fusion) protein
Pathogenesis: virus enters via nasopharynx, replicates in regional lymph nodes
-viremia follows, hematogenous spread
Disease:
1. German measles - mild fevers, rash on head and neck, spreads to body
resolves in 2-3 days, but contagious for 7 days
2. Congenital rubella syndrome - rubella acts as a teratogen → severe birth defects
don't give vaccine to women during pregnancy or within 3 months of conceiving
serology
spread by fecal-oral route
encodes 4 proteins - helicase, protease, RNA polymerase, capsid protein
can withstand heat and chlorination (swimming pools, disinfectants)
Pathogenesis: causes blunting of small intestinal villi, esp. jejunum
-virus shedding in stool highest in first 1-2 days
-extremely contagious!
Disease:
1. Gastroenteritis - vomiting and diarrhea, fever, myalgias, malaise; 2-3 days then done
clinical, epidemiological
diagnosis; ELISA
infections occur in winter and spring
virulence probably due to recombination event of 2 different coronaviruses
infects multiple species, cats, dogs, etc - spread by respiratory droplets and other secretions
Disease:
1. SARS - 2-7 day incubation, but up to 10 days - important for sequestering possible pts
a) fever - then chills, headache, malaise, maybe diarrhea
b) dry cough, shortness of breath, which may rapidly progress to respiratory distress that
requires mechanical assistance
-CXR shows increasing infiltrates and consolidations
-lymphopenia, thrombocytopenia, elevated creatinine and LFT's
clinical diagnosis
viral cultures and PCR
being tested now;
ELISA (+) after 1 month
symptomatic
live attenuated vaccine
part of MMR
supportive treatment
with fluids
no vaccine
supportive treatment
no vaccine
VIRUS
Human
Immunodeficiency
viruse (HIV)
West Nile virus
FAMILY
Retrovirus
Flaviviridae
ENVELOPE
STUFF TO KNOW
yes
carries 2 identical copies of RNA and reverse transcriptase enzyme
ten billion virions are produced and destroyed each day; HIV is not latent!
-gp120 amd
viral set point reached at ~6 months, lose about 50 CD4 cells per year
gp41 most
Virulence:
important
-gag codes for internal structural proteins
-pol codes for reverse transcriptase, protease, integrase
-memory CD4 -env codes for gp120 (binds to and gp41
cells do not
-tat (transcription factor) binds RNA LTR sequence to enhance transcription
have viral
-rev regulates export of full genomic (unspliced) RNA
surface
-nef down-regulates host cell MHC class I and CD4 expression, enhances release of virus
proteins
(nef deletion results in much slower progression of disease)
-virion maturation is completed as it is budding off the host cell
Pathogenesis: acute infection - dendritic cell binds HIV with DC-SIGN receptor,
brings to lymph node, where extensive replication occurs
-gp120 binds to CD4 and CCR5/CXCR4, then gp41 inserts into membrane and allows
fusion with host cell
-clinical latency for up to 10 years or more - depends on immune response, HLA type, etc
Disease:
1. Acute HIV infection - fever, lymphadenopathy, macular rash, fatigue, sore throat
can treat at this stage to delay onset of AIDS
2. AIDS/Opportunistic infections - usually with CD4 counts under 200, reactivations of latent dz
a) TB: CD4 = 300
b) PCP: CD4 = 200
c) Toxoplasmosis: CD4 = 100
d) Cryptococcal dz: CD4 = 100 - diarrhea may be dominant symptom
e) M. avium complex: CD4 = 50 - diarrhea may be dominant symptom
f) CMV: CD4 = 50
g) cryptosporidium - diarrhea
yes
vector-borne disease - transmitted by mosquito bite, usually in late summer
previously described virus, but in new location
human-human transmission possible because of blood transfusions, organ transplantation,
and breast-feeding
single polyprotein made from RNA - encodes M (membrane), E (envelope) and many NS
(nonstructural) proteins
neurons don't express MHC class I, so CTL's can't kill infected neurons
Pathogenesis: mosquito bite leads to viral replication in peripheral sites
-viremia in blood follows, with eventual CNS invasion and disease
Disease:
1. Asymptomatic - most common
2. Flu-like illness, abrupt onset with fever, headache, sore throat, rash, lymphadenopathy
3. Encephalitis - flu-like syndrome progresses to encephalitis, with changes in mental status
and focal neurological abnormalities → profound muscle weakness prominent feature
-neuronal apoptosis induced by virus, CSF pleocytosis
-elderly at greatest risk; overall mortality ~5%
TREATMENT/
VACCINE
acute - use ELISA,
Western blot, and RNA
viral PCR
AIDS - use CD4 count
and RNA viral load
Treatment: almost
always triple combo!
Resistance if less
(see syllbus for combos)
no vaccine
clinical diagnosis
and serology
supportive treatment
(IFN + Ribavarin in
clinical trials)
no vaccine yet
VIRUS
Dengue virus
Yellow fever virus
FAMILY
Flaviviridae
Flaviviridae
ENVELOPE
yes
yes
STUFF TO KNOW
vector-borne disease - transmitted by mosquito bite, usually in late summer
most common arthropod-borne viral infection; worldwide distribution in warmer climates
same structure for all flaviviridae (see above)
same pathogenesis as above (mosquito bite, viremia, CNS invasion)
major exception - cross-protective immunity does not occur, reinfections are often worse!
Diseases:
1. Dengue fever (DF) encephalitis - 2-7 day incubation period
a) joint/bone pain, fever, headache, retro-orbital pain, then vomiting, respiratory symptoms
b) fever, rash, lymphadenopathy, cytopenia
-NO fatalities!
2. Dengue Hemorrhagic fever (DHF) - dengue-like illness with thrombocytopenia and
increased hematocrit - usually 2nd infection, but can be first
-increased vascular permeability = ↑ TNF, IL-8, apoptotic endothelial cell death
-bleeding diathesis = cytokines, vascular injury, viral antibodies to platelets
-circulatory failure with GI bleeding, pulmonary edema, neurological manifestations
-can lead to shock
-10% fatal if untreated, less than 1% fatal if treated
Reasons why re-infection is worse: pts have non-neutralizing antibodies to DF that will bind
the virus, and simply target it more efficiently to the Fc receptors on macrophages, where
it can replicate faster; this is called antibody-dependant immune enhancement
-also, memory CD4+ and CTL's results in increased cytolysis of Dengue-infected
macrophages, which results in much higher amounts of cytokines and vasoactive mediators
vector-borne disease - transmitted by mosquito, usually in late summer
same structure as above (flaviviridae)
occurs exclusively in Africa and Americas, not Asia - no human-human transmission
different mosquitos transmit different diseases - jungle yellow vs. urban yellow
Pathogenesis: mosquito bits leads to replication in regional lymph nodes, followed by
hematogenous dissemination and liver infection - degeneration and "Councilman bodies"
caused by direct viral injury
-vasoactive and inflammatory cytokines are released → hemorrhagic diatheses, shock
Disease:
1. Yellow fever - 3-6 day incubation period, 3 stages of disease
a) viremia - fever, chills, headache, back pain
b) remission, lasts 1 day
c) intoxication - jaundice, "black vomit" hematemesis, shock - no viremia
-in pts with jaundice, mortality is 20-50%
TREATMENT/
VACCINE
clinical diagnosis
supportive treatment
essential for survival;
Ribavarin?
vaccine becoming
available
serology, viral culture
no liver biopsy!
supportive treatment;
Ribavarin?
live attenuated vaccine
boosters given q. 10yrs
VIRUS
Measles virus
Prions
FAMILY
Paramyxoviridae
Prions
ENVELOPE
yes
(different)
STUFF TO KNOW
transmission via respiratory droplets
envelope contains HA and F proteins, virion also comes with RNA polymerase
Th2 response
Pathogenesis: virus infects epithelium of respiratory tract, spreads to local lymph nodes
-viremia follows, hematogenous spread
Disease:
1. Measles - 7-14 day incubation - fever, rhinitis, cough, conjunctivitis, photophobia
Koplik spots appear in the mouth, followed by rash on head and then trunk - not
contagious at this point
proteinaceous infectious particles
no genome, not inactivated by UV light, heat, or formaldehyde
Biology: PRPc is a normal human protein on chromosome 20. Infection results in PRPsc.
PRPc = It is α-helical, protease sensitive, located on cell surface
PRPsc = β-sheets, protease insensitive, located in cytoplasm
-insolubility b/c of protease insensitivity thought to cause storage problems and aggregation
Diseases: TSE = transmissible spongiform encephalopathies
1. Kuru - spread by exposure to brains/mucous membranes of infected individuals
headaches, arthralgias, neurologic disease and death within 3months - 1year
2. CJD (Creutzfeldt-Jakob disease) - can be sporadic or from infected surgical instruments
vCJD = mad cow disease (variant); death within 3-6 months
-looks like Alzheimer's disease, lack of coordination, dementia, motor weakness
3. Fatal familial insomnia - autonomic dysfunction and sleep disturbances
thalamic, cerebellar changes
4. Gerstmann-Straussler-Scheinker (GSS) disease - autosomal dominant,
progressive spinocerebellar degeneration and accumulations of plaques in cerebellum
TREATMENT/
VACCINE
Koplik spots are
diagnostic
symptomatic treatment
Ribavarin?
live attenuated vaccine
part of MMR - 2 doses are
recommended
clinical syndromes,
history
no treatment